Faecal transplant used to treat inflammatory bowel disease in mice
Changes in the composition of gut microbes is responsible for inflammation of the intestines in inflammatory bowel disease (IBD), said scientists from the Netherlands and the US – which can apparently be overcome through faecal transplants. Led by microbiologist Dr. Sahar El Aidy from the University of Groningen in the Netherlands, a team of scientists found changes of the gut microbial composition caused by the absence of the antimicrobial compound catestatin in mice with IBD.
In normal mice, catestatin is secreted by cells lining the gut and kills susceptible bacterial strains.
The scientists used faecal transplants in a group of mice genetically engineered to lack catestatin (knock-out mice) and in a group of normal mice, in order to find the cause of inflammation typical of IBD. Both groups of mice were given a laxative that removed most of the bacteria from their intestines instead of antibiotics, which could hamper recolonisation after the faecal transplant.
The results revealed that the microbial composition in the intestines had shifted towards that of the donor, indicating successful faecal transplants. Further, analysis of the metabolites inside the gut showed that the production of short-chain fatty acids, molecules that affect the function of the gut, was reduced in the knock-out mice.
“The reduction in short-chain fatty acid production was the result of a change in the microbial community in the intestines, which was in turn caused by the absence of catestatin,” explained Dr. El Aidy. “Our experiments showed that the epithelial permeability of the intestines, which is higher in the knock-out mice, is restored by the faecal transplant. Also, the extent of fibrosis resulting from inflammation was reduced.”
However, the scientists do not plan to treat human patients with faecal transplants because of contradictory outcomes.
Instead, the results from the new study have given the scientists a clear target to specific bacterial strains that are affected by the removal of catestatin, a school of thought which was missing in previous attempts to restore a healthy intestinal microbial community
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